How ‘love hormone’ could help heart attack patients

By Mark Waghorn via SWNS

A chemical released from love could treat heart attack patients, according to new research.

Oxytocin, dubbed the "love hormone," helps heal the heart by boosting the production of stem cells.

The findings are based on human tissue grown in the lab and experiments on zebrafish - which have a remarkable ability to repair themselves.

Study senior author Dr. Aitor Aguirre, of Michigan State University, said: "Here we show oxytocin, a neuropeptide also known as the love hormone, is capable of activating heart repair mechanisms in injured hearts in zebrafish and human cell cultures.

"It opens the door to potential new therapies for heart regeneration in humans."

Oxytocin stimulates erections and orgasms. In women, it is believed to help sperm reach the egg.

The chemical is produced by the hypothalamus in the brain. It is secreted by the pituitary gland.

Abnormal amounts have been linked to sex addiction. It is behind many pleasurable feelings - from art and exercise to lovemaking.

The researchers found it also causes stem cells from the heart's outer layer, or epicardium, to migrate into the middle, known as the myocardium.

There they develop into cardiomyocytes, muscle cells that generate heart contractions. The discovery offers hope of promoting regeneration.

They die off in great numbers after a heart attack. Highly specialized cells don't replenish themselves.

But previous studies have shown a subset called EpiPCs (Epicardium-derived Progenitor Cells) can undergo reprogramming - becoming cardiomyocytes or other types of heart cells.

Dr. Aguirre said: "Think of the EpiPCs as the stonemasons that repaired cathedrals in Europe in the Middle Ages."

Production is inefficient for heart regeneration in humans under natural conditions. But the humble zebrafish may hold the key.

They are famous for their extraordinary capacity for regenerating organs including the brain, retina, internal organs, bone and skin.

Zebrafish can regrow their heart when as much as a quarter of it has been lost.

This is done by the proliferation of cardiomyocytes and EpiPCs. And the 'magic bullet' appears to be oxytocin.

In zebrafish, within three days after the heart was exposed to 'cryoinjury' by freezing, expression of oxytocin in the brain soared twentyfold.

Scans showed the hormone traveled to the epicardium and bound to the oxytocin receptor. This triggered a molecular cascade, stimulating local cells to expand and develop into EpiPCs.

The new cells headed for the zebrafish myocardium to develop into cardiomyocytes, blood vessels and other important heart cells, to replace those which had been lost.

Crucially, the researchers found oxytocin has a similar effect on cultured human tissue. It turned human Induced Pluripotent Stem Cells (hIPSCs) into EpiPCs.

Numbers doubled with the hormone. None of 14 other brain hormone tests conducted worked.
The effect was much stronger than other molecules tried in mice.

On the other hand, genetic engineering that knocked out the oxytocin receptor prevented the regenerative activation of human EpiPCs.

The link between oxytocin and the stimulation of EpiPCs was identified in a chemical pathway known to regulate the growth, differentiation and migration of cells.

Dr. Aguirre said: "These results show it is likely the stimulation by oxytocin of EpiPC production is evolutionary conserved in humans to a significant extent.

"Oxytocin is widely used in the clinic for other reasons, so repurposing for patients after heart damage is not a long stretch of the imagination. Even if heart regeneration is only partial, the benefits for patients could be enormous."

He added: "Next, we need to look at oxytocin in humans after cardiac injury. Oxytocin itself is short-lived in circulation, so its effects in humans might be hindered by that.

"Drugs specifically designed with a longer half-life or more potency might be useful in this setting.

"Overall, pre-clinical trials in animals and clinical trials in humans are necessary to move forward."

The study is in Frontiers in Cell and Developmental Biology.